Objective: A comprehensive study of the induction of lymphatic leukemias, lymphomas, and other neoplasms resulting from interactions among external leukemogens (ionizing radiation and certain chemicals), the radiation leukemia virus (RadLV), the lymphoid cells which are the targets for its oncogenic activity, the thymus epithelium, the bone marrow, and the genetic, immunologic, and physiologic environment provided by strain C57BL mice and other rodent hosts. Both in vivo and in vitro methods will be utilized to elucidate the following specific topics: (1) genetic control of RadLV replication in vitro; (2) evidence for repression and depression of the viral genome; (3) kinetics of RadLV replication and maturation in vitro; (4) mechanisms of induction of viral replication by X rays in vivo and by BUdR in vitro; (5) cell type as a determinant of the attenuation of leukemogenicity of RadLV in vitro; (6) modulation of viral coat proteins by cell passage history; (7) RNA-DNA hybridization studies; (8) isolation, characterization, and complementation studies of temperature-sensitive viral mutants; (9) differentiated state of the target cell as a determinant of viral oncogenicity; (10) differentiated states of heterokaryons and fused cell hybrids as determinants of capacity for viral replication; (11) attempted conditioning of RadLV-infected target cells to undergo neoplastic transformation in vitro; (12) conditioning role of the thymus epithelium in vivo; (13) immune sanctuary role of the thymus, brain, and selected other tissues for virus-infected target cells; (14) further characterization of cellular and viral antigens; (15) immune fluorescence studies of time course of evolution of gs antigen in unirradiated and irradiated C57BL mice; (16) attempted rescue of an endogenous sarcoma virus genome from transformed and untransformed C57BL mouse embryo fibroblasts in vitro; (17) quantitative dose-response studies of the inactivation of various RadLV functions by UV and X rays.